The debate goes like this .If stable angina can present with equivalents ? what prevents “Unstable angina” to present with Anginal equivalents without chest pain ?

If a diabetic patient who had a silent MI in the past . . . subsequently experience severe episodes of resting ischemia , will he feel the pain , that is supposed to occur with his “unstable angina” or not ?

Hmm , difficult to guess right, So it seems highly plausible UA/NSTEMI do occur silently ! Literature hasn’t looked into this specifically. Chest pain is built integral into definition of UA , infact it is a symptom complex rather than an disease entity by itself, while NSTEMI is ECG and enzyme combo ! Making the term NSTE-ACS look perfect.

Any other technical explanation ?

The concept of Ischemic cascade says angina occurs last, well after biochemistry , wall motion defect and ECG , hence its distinctly possible for UA/NSTEMI present to be painless !

Final message

Anginal pain perception is related to intactness of neurogenic circuits and also probably the severity of Ischemia.If full thickness myocardial necrosis can be painless in few, nothing prevents from an episode of UA/NSTEMI be truely painless .

Clinical implication of this conundrum

Can we admit a patient as UA/NSTEMI with out chest pain ?

Yes, it would seem so .

No, we can’t .

Indeed we can , if ECG changes are there .

No, we can admit even with normal ECG if its real unstable angina.

This is the crux of the problem in ERs all over the globe. Our knowledge base is simply not good enough. Every one of us has seen Troponin positive silent NSTEMIs ! but . . . to me still something is missing in the link .

Modern day approach

Pain or no pain,any fresh ECG changes ( Both T and ST shifts*) should be rushed to cath lab.Whenever you are not sure .Always better to err on the side of over investigation.That’s the mantra ! So ,you do an Angiogram , find an Incidental intermediatroy lesion which may not be responsible for the ECG changes but you are compelled to go after it FFR//iFR , OCT, IVUS and so on !

*There is huge list of non Ischemic ST/T shifts in ECG that can be read elsewhere .

Counterpoint

Can’t agree with this article. Foolish to diagnose UA without chest pain. Never treat ECG in isolation unless its a convincing ST elevation or depression with clinical input and thorough scrutiny of past record . Realise , how important is the basics principles of medicine taught by Oslers and Cushings a century ago.

What prevents the neck pain of cervical spinal disease to be referred over the heart ? Can pure spinal lesions mimic angina ?

The answer seems to be “Yes” . The neuronal circuit is there .Only , the traffic has to be reversed. Medical logic is always puzzling. There is indeed an entity called cervical angina.

The cardiac pain can be referred any where between dermatomes C3 to T 10 It is generally believed cervical radicular pain can go only one way . . . ie towards the nape of neck and arms .Dermatomal overlap ,neural cross talks thalamic inputs and cortical reflection and perception always make the subject of referred pain too complex.

Now,It seems possible ,the neck pain can spill over into the anterior chest wall ,mimicking angina .Imagine the confusion if the patient has both cardiac and cervical entities ! Does the pain signals from the two sites collide in the local spinal network ? Does one extinguish or amplify the other ?

Stable angina is graded by Canadian cardiovascular society classification ( CCSC ) by 4 grades. Angina at rest usually denotes unstable angina. But, patients with stable angina may also experience rest angina according to CCSC , still this is not considered as unstable angina by many . Post prandial angina is one such example.

Few consider post prandial angina as unstable angina . This sort of reasoning can not be faulted .

In the logical sense , we are dealing with varied categories of unstable angina. The importance of diagnosing unstable angina is to intervene early , so that we can avoid major adverse outcome .

The problem in CAD is , often , the plaques and angina do not obey the conventional rules !

.The following permutations and combinations could be observed in any coronary care unit .

Unstable angina – stable plaques – stable ECG – stable patient

Unstable angina – unstable plaques – unstable patient

Unstable Angina – unstable plaque – stable patient

Stable Angina – unstable plaque – unstable patient

Stable angina – stable plaque – stable patient

Stable angina – unstable plaque – stable patient

Among the above 6 categories 2nd is probably the most dangerous group and category 5 is most benign.

Post prandial angina is a serious form of angina.It implies , even diversion of little blood to GI system immediately after a meal can provoke an episode of ischemia .This infers a very tight lesion somewhere in the coronary tree, very often it could be the left main or proximal LAD.

Of course , there is another mechanism for post prandial angina, namely GI neurotransmitters like gut peptides acting as a coronary vasoconstrictor.

Snippets on post prandial angina .

It is also recognised , post prandial angina occurs more often during dinner, followed by lunch and breakfast. Carbohydrate foods are more likely to precipitate it .

Does PPA cause ST depression ?

Logically it should .In reality It happens in few .

How to manage it ?

It is very important to recognise , even though this article argues for including PPA as UA, there is no acute thrombotic process during an episode of post prandial angina . In fact , it is more of a secondary UA due to altered blood flow pattern.

So , do not admit these patients in CCU and administer heparin or 2a 3b blockers. (Unless of course ,they have other forms of rest angina )

Post prandial angina has all the characters of a severe form of angina .There is every reason to label it as UA .It is suggested , ACC,ESC, AHA should consider including post prandial angina as UA or at least UA equivalent .This would help intervene this entity early.

Pulmonary embolism is one of the important causes of acute chest pain . It can mimic acute coronary syndrome . In fact along with aortic dissection , it forms a differential diagnosis for STEMI especailly if the ECG is not typical.

The Chest pain of acute pulmonary embolism can originate in one of the following structures with different mechanism

Lung parenchyma ( Necrotic pain ?)

Pluritic pain in adjacent necrotic segment

Main Pulmonary artery and it’s branches

Right ventricular mechanical stretch

Right ventricular ischemia

Hypoxia induced LV ischemia with coexisting CAD.

Multiple contribution from any of the above *

It should also be remembered , medicine never respects logic, as some times an episode of pulmonary embolism can occur without any chest pain

Localisation of chest pain

One can imagine , how difficult for the nervous system to zero in on the origin of this pain as the structures involved in acute pulmonary embolism are in different planes and in different depths within the chest cavity . Patients often complain vaguely the site of pain but what is universal is severe resting pain deep within the chest . If the ischemic lung segment transmit pain signals , the location and radiation depend on the bronchpulmonary segment involved.This again adds on to the complexity in the genesis of pain .It can be virtually any where in the back or front of chest.

But , the central and retrosternal chest pain are equally common as invariably the central pulmonary arteries go for a acute stretch which can be severely painful .In fact , current thinking is it could contribute maximum for the intensity of chest pain. Similarly, acute dilatation of RV result in mechanical pain. RV sub endocardial ischemia may also contribute .An intact bronchial circulation( From aorta) can limit the ischemic lung pain .

Final message

Analysing the chest pain of acute pulmonary embolism can be an interesting academic exercise . It could arise from multiple structures with different mechanisms. It may not be much significant with reference to management . But it has a diagnostic role. A pain which is severe , and atypically located should raise the suspicion of acute PE especially if the patient has associated dyspnea.

Coronary arterial spasm is a commonly discussed entity in clinical cardiology. Originally described by prinzmetal decades ago .It was reported to occur only in coronary care units as variant angina .There is nothing called stable spasm every episode of spasm is considered as unstable angina.

How common is coronary artery spasm ?

This condition thought to be very common during ACS , but notoriously difficult to confirm.In fact many of episodes are clinically suspected and never confirmed. There has been lot of provocative tests for confirming coronary spasm like ergonavine etc.None of these tests were neither useful nor practical.

What are the clinical situations where coronary spasm occur ?

Old concepts die hard.Most of us believe , the most common cause for coronary spasm is prinzmetal’s angina ie , angina in normal coronary arteries or with minimal lesions .Clinical experience , has taught us coronary spasm can occur in all spectrum of acute coronary syndrome or even chronic coronary syndromes.

Some believe every episode of STEMI will have a component of coronary spasm.

In NSTEMI/Unstable angina spontaneous coronary spasm is an important pathogenetic mechanism

Now, we witness transient coronary artery spasm in the cath lab due to catheter and other hard ware.The spasm here , is secondary to mechanical stress and this in no way related to the coronary spasm described by prinzmetal in the pre cath era.

What is the link between coronary spasm and electrocardiogram ?

The most common fallacy among coronary care physician is , if it is spasm there must be ST elevation

The classical cardiology teaching all over the world , has been so powerful this myth continues to prevail over . The fact of the matter is , the coronary arterial spasm , can never have any direct impact on the ECG. (Unless , coronary smooth muscle generate ST currents !) . So , whatever be the effect of spasm it is through it’s effect on the myocardial blood flow.

Hence , it is not the coronary artery spasm that will dictate the movement of ST segment . It is the impact of myocardial blood flow to the layers of the myocadium namely , endocardium, epicardium , epicardium ( or a combination of the above ) that will dictate ST segment dynamics.

Among this , the most common manifestation of coronary spasm is thought to be , subendocardial ischemia and resultant ST depression .This classically occur in many cases of NSTEMI/UA .

This makes ST depression the dominant manifestation of spasm ,

How coronary spasm can elevate the ST segment ?

If it can induce a transmural ischemia it can elevate a ST segment . Does all episodes coronary spasm result in transmural ischemia ? No,not at all .in fact it happens very rare as we have already seen .

To result in transmural ischemia , the spasm should be total & sustained , at least for few minutes to completely occlude the blood flow .

Milder forms of spasm can elicit only a sub endocardial ischemia that depress the ST segment.

*There is a rare variety of spasm where subepicardium is more affected than endocardium and hence ST elevation may occur.

What is the effect of Nitroglycerine on coronary spasm ?

This is a very powerful coronary spasmolytic agent.We can witness it’s action more vividly in cath lab .

It brings back the ST segment to neutral position , from either a elevated or depressed state .Many believe , ( may it’s a fact ) much of the early benefit of angina relief in UA/NSTEMI is amelioration of coronary spasm

Is coronary spasm a neural event or a biochemical event ?

The exact answer is not known .It should be chemicals as neural signals are also mediated by chemicals.

What are the biochemical mediators of coronary spasm ?

Smooth muscle calcium : Calcium flux is the immediate cause for spasm

Mediators .Neural :Catecholamine ,

Thrombus secretes Thromoxane A2 which is a powerful vasoconstrictor

Smooth muscle calcium

Is coronary vasoconstriction and coronary spasm are synonymous ?

Both terms are synonymous . Vasoconstriction is often used to refer constriction of microvasculature

while spasm often describes the event in large epicardial vessel. Some times the term coronary vasomotion is used to describe fluctuating coronary arterial tone.

It is thought to be rare. Even in prinxmetal series some amount of atherosclerosis was documented in most patients.

What is the relationship between spasm and adjacent lesion ?

Spasm following PCI :Can spasm crush a stent ?

Can a coronary collaterals go for spasm ?

Logically Spasm can occur coronary collaterals .But it is difficult to document .coronary collaterals eventhough has three layes as that of artery (Intima, media, adventia) th medial smooth muscles are less sparse. Advential lack vasa nervorum and hence neural input is less.So spasm is a rare event in coronary collaterals

NSTEMI constitutes a very heterogeneous population .The cardiac risk can vary between very low to very high . In contrast , STEMI patients carry a high risk for electro mechanical complication including sudden death .They all need immediate treatment either with thrombolysis or PCI to open up the blood vessel and salvage the myocardium.

The above concept , may be true in many situations , but what we fail to recognize is that , STEMI also is a heterogeneous clinico pathological with varying risks and outcome !

Let us see briefly , why this is very important in the management of STEMI

Management of STEMI has undergone great change over the past 50 years and it is the standing example of evidence based coronary care in the modern era ! The mortality , in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15% in 1960 /70s . Early use of heparin , aspirin further improved the outcome .The inhospital mortality was greatly reduced to a level of 7-8% in the thrombolytic era. And , then came the interventional approach, namely primary PCI , which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence for the superiority of PCI , it is only a fraction of STEMI patients get primary PCI even in some of the well equipped centers ( Could be as low as 15 %)

Why ? this paradox

Primary PCI has struggled to establish itself as a global therapeutic concept for STEMI , even after 20 years of it’s introduction (PAMI trial) . If we attribute , lack of infrastructure , expertise are responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world , reluctant to do primary PCI for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI patients !

All STEMI’s are not same , so all does not require same treatment !

Common sense and logic would tell us any medical condition should be risk stratified before applying the management protocol. This will enable us to avoid applying “high risk – high benefit” treatments in low risk patients . It is a great surprise, the cardiology community has extensively researched to risk stratify NSTEMI/UA , it has rarely considered risk stratification of STEMI before starting the treatment.

In this context , it should be emphasized most of the clinical trails on primary PCI do not address the clinical relevance and the differential outcomes in various subsets of STEMI .

Consider the following two cases.

Two young men with STEMI , both present within 3 hours after onset of symptoms

In the above example, a small inferior MI by a distal RCA occlusion , and a proximal LAD lesion jeopardising entire anterior wall , both are categorized as STEMI !

Do you want to advocate same treatment for both ? or Will you risk stratify the STEMI and treat individually ? (As we do in NSTEMI !)

Current guidelines , would suggest PCI for both situations. But , logistic , and real world experience would clearly favor thrombolysis for the second patient .

Does that mean, the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a random basis by not so well experienced cath lab team.

(Note : Streptokinase or TPA does not vary it’s action , whether given by an ambulance drive or a staff nurse or even a cardiologist ! .In contrast , the infrastructure and expertise have the greatest impact on the success and failure of PCI )

Final message

So , it is argued the world cardiology societies(ACC/ESC etc) need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

Angina is classified in many ways .The most useful , clinical classification is stable and unstable angina . While ,the former generally is considered innocuous the later conveys a sinister signal to the patient as well as the physician.

Why stable angina is stable ?

In stable angina

The patient knows how the pain is going to behave by his past experience.

Very predictable .The patient knows at what distance it’s going to come

He also knows when it will disappear.(For some , with rest for others with nitrates)

He also knows where the chest pain will radiate.

If some thing is unusual it is unlikely to be stable angina , also any first episode of angina is considered unstable as one wouldn’t know how the angina is going to behave !

How is that stable angina has such a learned behaviour ?

The main reason for the beningn nature of stable angina is the coronary artery has “stable plaques”

Stable plaque s restrict blood flow only at times of increased demand( ie supply side ischemia.) There is no thrombus in these plaques.As soon as the exertion ends the angina is relieved.So in chronic stable angina, the patient is stable, the angina is stable , the palque is stable , the coronary blood flow is stable.

Unstable palques have erosion and thrombus , and it interferes with blood flow even at rest .So in unstable angina, not only the angina is unstable , the plaque is unstable ,coronary blood flow is unstable. So it is obvious unstable angina , may not be relieved by bed rest.It needs intensive treatment.